Overtraining syndrome (OTS) occurs where an athlete is training vigorously, yet performance deteriorates. One sign of OTS is suppressed immune function, with an increased incidence of upper respiratory tract infection (URTI). An increased incidence of URTIs is also associated with high volume/intensity training, as well as with excessive exercise (EE), such as a marathon, manifesting between 3-72 hours post-race. Presently, there is no encompassing theory to explain EE and altered immune competence. Recently, it has been conclusively established that T helper lymphocytes (T(H)), a crucial aspect of immune function, represent two distinct functional subsets: T(H)1 and T(H)2 lymphocytes. T(H)1 lymphocytes are associated with cell-mediated immunity (CMI) and the killing of intracellular pathogens, while T(H)2 lymphocytes are associated with humoral immunity and antibody production. When T(H)-precursor cells are activated, the balance is tipped in favour of one or the other. Furthermore, the most appropriate means of determining the T(H)-subset, is by the prevailing cytokine 'pattern'. This paper hypothesises that exercise-related immunosuppression is due to tissue trauma sustained during intense exercise, producing cytokines, which drive the development of a T(H)2 lymphocyte profile. A T(H)2 cell response results in simultaneous suppression of CMI, rendering the athlete susceptible to infection. Additionally, increased levels of circulating stress hormones (cortisol and catecholamines), as well as prostaglandin E(2), support up-regulation of T(H)2 lymphocytes. Marathon-related data are presented to support this hypothesis. It is concluded that an increased incidence of illness associated with OTS and in response to EE is not due to immunosuppression per se, but rather to an altered focus of immune function, with an up-regulation of humoral immunity and suppression of CMI.